View source for Schoepf 2019 MitoFit Preprint Arch

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{{Publication
|title=Schöpf B, Weissensteiner H, Schäfer G, Fazzini F, Charoentong P, Naschberger A, Rupp B, Fendt L, Bukur V, Eichelbrönner I, Sorn P, Sahin U, Kronenberg F, Gnaiger E, Klocker H (2019) OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and a prognostic gene expression signature. https://doi.org/10.26124/mitofit:190003 - ''2020-03-20 published in [[Schoepf 2020 Nat Commun |»Nature Communications 11:1487«]]''
|info=MitoFit Preprint Arch 2019.3. [[File:MitoFit Preprint Arch pdf.png|left|160px|link=http://www.mitofit.org/images/d/dc/Schoepf_2019_MitoFit_Preprint_Arch.pdf |MitoFit pdf]] '''[http://www.mitofit.org/images/d/dc/Schoepf_2019_MitoFit_Preprint_Arch.pdf OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and a prognostic gene expression signature]'''
<br />

|authors=MitoFit Prep 2019.3.
|year=2019
|journal=MitoFit Prep
|abstract=Version 1 ('''v1''') '''2019-06-11''' [http://www.mitofit.org/images/d/dc/Schoepf_2019_MitoFit_Preprint_Arch.pdf doi:10.26124/mitofit:190003] - <big>'''2020-03-20 Published in [[Schoepf 2020 Nat Commun |»Nature Communications 11:1487«]]'''</big>
 
Rewiring of energy metabolism and adaptation of mitochondrial respiratory functions are considered to impact on prostate cancer development and progression. High-resolution respirometry of paired benign and malignant human prostate tissue samples revealed reduced respiratory capacities with NADH-pathway substrates glutamate and malate in malignant tissue and a significant metabolic shift towards respiratory capacity with succinate, particularly in high-grade tumors. The load of potentially deleterious mitochondrial-DNA mutations was higher in tumor tissue and associated with unfavorable risk factors. High levels of potentially deleterious mutations in mitochondrial Complex I-encoding genes were associated with a 70% reduction in NADH-pathway capacity and compensation by increased S-pathway capacity. Structural analyses of these mutations revealed amino acid alterations leading to potentially deleterious effects on Complex I, supporting a causal relationship. RNA-seq revealed a signature of metabolic enzymes corresponding to the altered mitochondrial respiratory pathways and enabled extraction of a metagene set for prediction of shorter disease-free survival.
|keywords=Mitochondria, high-resolution respirometry, oxidative phosphorylation, mitochondrial DNA mutation, mtDNA heteroplasmy, metabolic reprograming
|editor=[[Gnaiger E]],
|mipnetlab=
}}
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== Preprints for [[Gentle Science]] ==
{{MitoFit preprint}}